Letter to the Editor

摘要

We read with interest the recent article by Lori D Hill and colleagues titled, 'Catechol-O-Methyltransferase (COMT) single nucle-otide polymorphisms and haplotypes are not major risk factors for polycystic ovary syndrome.' This renewed interest in the role of COMT and estrogen metabolism in pathogenesis of polycystic ovary syndrome (PCOS) is largely built on our earlier publications (Salih et al., 2007,2008). In these publications we have shown that women with PCOS have lower urinary 2-hydroxyestrogen levels (Salih et al., 2007) and an increased expression of COMT protein in the granulosa cells (Salih et al., 2008). Although it is plausible that increased COMT expression in PCOS could be due to specific single nucleotide polymorphisms (SNPs) in gene regulatory region, as elegantly investigated in the Hill et al., manuscript, it is more likely due to external gene modifiers. In fact, we have shown that dihydrotestosterone, insulin and ATRA, well known to be elevated in PCOS patients (Gilling-Smith et al., 1994; PCOS, 2004; Wood et al., 2004), upregulate COMT expression (Salih et al., 2008). It was also suggested that the increased expression of COMT with a subsequent increase in the level of COMT product 2ME (2 meth-oxyestradiol) in granulosa cells may lead to ovulatory dysfunction, follicular arrest and aberrations in steroidogenesis which are hallmarks of PCOS.